The bioinformatic prediction revealed that TP53 was a putative target gene of miR-612 and CD40 of miR-1976. Moreover, TP53 was downregulated in the expression array when comparing HR vs LR expression levels adjusted by sex, diet, age and baseline weight, and CD40 showed a statistical trend.

The expression of COX-2 increase with stage of the endometrial tumor and with the expression of p53 and VEGF in the endometrial carcinomas.

Study results revealed that the expression of LOC285194 was significantly lower in non-small cell lung cancer (NSCLC) tumor tissues when compared with the corresponding non-tumor tissues. Its expression was correlated with the tumor size, disease-free survival, and overall survival rates. RNA protein interaction analysis revealed that p53 was the direct binding target of LOC285194 in NSCLC.

This review provides a systematization of the p53 influence on glycolysis and oxidative phosphorylation (OXPHOS), giving attention to the interplay of p53 with key signaling pathways, including c-Myc, HIF-1, LKB1/AMPK, and PI3K/Akt, as well as to mutant p53 gain-of-function. It also contributes to a better understanding of distinct metabolic profiles in heterogeneous tumor cell populations. [review]

Results show the oligomerization of p53 during activation by CK2 phosphorylation at Ser392 in the presence of ATP. This process increased levels of PAb1620 and masks the cryptic epitopes of PAb240 and DO12, increasing native conformation. Also, a stable complexes of CK2 and p53 are formed only in the presence of ATP and in the absence of DNA.

It was suggested that the transfection of miR-126 mimics could inhibit the telomere-p53-p21-Rb and JAK/STAT signaling pathway activity in vitro and delay the senescence of HGMCs. The results may serve as a new strategy for the treatment of Diabetic kidney disease

Low TP53 expression is associated with glioma.

Data reveal a GOF effect of p53 mutants in hypoxic tumors and suggest synergistic activities of p53 and HIF-1. These findings have important implications for cancer progression.

in a pig model of human familial adenomatous polyposis, p53 plays a role in the early precancerous stages of polyp development

Knockdown of p53 led to three outcomes: 1) cell death was attenuated; 2) Tunicamycin-induced redistribution of GRP78 from the nucleus to the endoplasmic reticulum lumen was recovered; and 3) the endoplasmic reticulum-fluorescence/EGFP-calreticulin was recovered.

This study demonstrated that various expression levels of p53 in porcine fibroblasts could be achieved by gene targeting and RNA interference.

SIRT1, p53 and NF-kappaB are involved in the control of both the proliferation and the apoptosis of ovarian cells.

Taken together, these results demonstrated that transmissible gastroenteritis virus infection promoted the activation of p38 MAPK and p53 signalling, and p53 signalling might play a dominant role in the regulation of cell apoptosis.

role of transcription factor p53 and the metabolic hormone leptin, in controlling basic functions (proliferation, apoptosis and secretory activity) of ovarian cells

CONCLUSION(S): (1) Apoptosis is involved in follicular atresia; (2) Bcl-2 is induced by warm ischemia; and (3) cryopreservation insult does not alter the apoptotic signals with short tissue preparation time.

Suppressive effect of FSH and LH on p53 expression and caspase-3 activity with parallel increase in bcl-2 expression and increased P production was observed.

p53 signaling might be a major determinant for the replicative senescence in the miniature pig fibroblast cells that have the shorter lifespan and slower growth rate compared to primary domestic pig fibroblast cells in vitro.

exogenous in vivo NO treatment seems to preserve VSMC from mitochondrial-dependent apoptosis and drive cells to quiescence through p53 increase

Rabbit Tumor Protein P53 (TP53) interaction partners

Suppressing expression of p53 was a required event in two assays of proliferative vitreoretinopathy.

These results suggest that p38 MAPK signal transduction pathway is critical to NO-induced chondrocyte apoptosis, and p38 plays a role by way of stimulating NF-kappaB, p53 and caspase-3 activation.

Our data indicate that exposure to rabbits to Pb(Ac)(2) caused a significant increase of apoptosis protein p53 and decrease in the antiapoptotic BCl2 proteins.

In the hsf4(null) fish, both p53 and activated-caspase3 were significantly decreased. Combined with the finding that the denucleation defect could be partially rescued through microinjection of p53, fas and bax mRNA into the mutant embryos, we directly proved that HSF4 promotes lens fiber cell differentiation by activating p53 and its downstream regulators

C/ebpalpha plays a role in liver growth regulation via the p53 pathway.

Results demonstrate a novel role of Klf8, achieved via modulation of p53 and met expression, in the maintenance neuronal progenitors and development of Purkinje cells and the proliferation of granule cells in the cerebella of zebrafish embryos

p53 has a limited role in eliciting the anemia phenotype of zebrafish models of Diamond-Blackfan anemia.

p53 protein accumulates during tumor formation as a result of tumor-specific inactivation of the Mdm2 pathway.

Data suggest that the co-inhibition of Tp53 activity rescued the morphological deformities but did not alleviate the erythroid aplasia indicating that ribosomal protein deficiency causes erythroid failure in a Tp53-independent manner.

Cow (Bovine) Tumor Protein P53 (TP53) interaction partners

The effect of p53 expression on the development of cloned embryos, and its interaction with HDAC1 and DNMT3A are reported.

Bov-A2 insertion into the TP53 promoter in Antilopinae and Tragelaphini may not only provide a genetic network that regulates mammary involution, but can also answer the need for rapid mammary involution in Savanna antelopes

Results demonstrate that embryonic developmental potential is related to the time of first cleavage and that p66(shc), but not p53, is up-regulated in early arrested in vitro-produced bovine embryos.

Mouse (Murine) Tumor Protein P53 (TP53) interaction partners

indicating a general perturbation of the p53, miR-34a and SIRT1 pathway in Huntington's disease

Using Fanca(-/-) HSCs expressing the separation-of-function mutant p53(515C) transgene, which selectively impairs the p53 function in apoptosis but keeps its cell-cycle checkpoint activities intact, we show that the p53 cell-cycle function is specifically required for the regulation of Fanca(-/-) HSC proliferation.

lipid profiles are significantly altered by the lack of p53 in muscle tissues.

p53 becomes activated in BM endothelial cells upon hematopoietic stresses such as irradiation and chemotherapeutic treatments. The conditional activation of p53 induces the expression of p53 target genes specifically in vascular endothelial cells, resulting in the dilation and collapse of vascular endothelial cells, reductions in perivascular mesenchymal stromal cells, and depletion of HSCs.

p53R245W tumors are the most aggressive and exhibit metastases to lung and liver.

L3MBTL2 plays a protective role in kidney injury, in part by inhibiting the DNA damage-p53-apoptosis pathway.

results indicate that miR-148b-3p contributes to the regulation of hypoxia/reoxygenation-induced cardiomyocyte apoptosis in vitro through targeting SIRT7 and modulating p53-mediated pro-apoptotic signaling

Results show an association of PD with p53 and active caspase-3 overexpression and beta-adrenergic receptor underexpression in the heart, potentially promoting the cardiac autonomic dysfunction frequently observed in PD.

findings uncover a new function of p53 in the regulation of Akt signaling and reveal how p53, ASS1, and Akt are interrelated to each other.

Xenopus laevis Tumor Protein P53 (TP53) interaction partners

The stabilities of the full-length p53 orthologs were marginal and correlated with the temperature of their organism, paralleling the stability of the isolated DNA-binding domains.

PP2A:B56{epsilon}, a substrate of caspase-3, regulates p53-dependent and p53-independent apoptosis during development.

Furthermore, while activities to process procaspase-8 and procaspase-9 appeared in SAMDC-overexpressed apoptotic embryos, the activity to process procaspase-8 did not appear in p53-overexpressed apoptotic embryos. [SAMDC]

XFDL156 actively restricts mesodermal differentiation in the presumptive ectoderm by controlling the spatiotemporal responsiveness to p53.

Horse (Equine) Tumor Protein P53 (TP53) interaction partners

Expression of p53 and Ki67 and presence or expression of EcPV2 and EcPV3 do not appear to be important prognosticators.

The allele frequency in Thoroughbred horse mares at codon 72 in exon 4 was 73.3% Arg/Pro, 17.1% Arg/Arg, 9.6% Pro/Pro. Presence of Arg/Pro was significantly associated with abortion, while Pro/Pro mares had a lower probability of abortion.

levels of p53 in rainbow trout tissues and cell lines reported; detection of high p53 levels in gills may reflect need for elevated checkpoint readiness in a tissue that would be expected to be accessible to genotoxic compounds in the aquatic environment

Medaka Tumor Protein P53 (TP53) interaction partners

p53 (TP53) profil antigène

Antigen Summary

This gene encodes a tumor suppressor protein containing transcriptional activation, DNA binding, and oligomerization domains. The encoded protein responds to diverse cellular stresses to regulate expression of target genes, thereby inducing cell cycle arrest, apoptosis, senescence, DNA repair, or changes in metabolism. Mutations in this gene are associated with a variety of human cancers, including hereditary cancers such as Li-Fraumeni syndrome. Alternative splicing of this gene and the use of alternate promoters result in multiple transcript variants and isoforms. Additional isoforms have also been shown to result from the use of alternate translation initiation codons (PMIDs: 12032546, 20937277).